In April, the National Institutes of Health announced new treatments to inhibit the advancement of Alzheimer’s disease. These have made possible blocking a regular protein called CD33, and therefore allowing support cells in the brain to clear away toxic plaques.
Post-mortem human brain research shows that CD33 protein is overactive in cases of Alzheimer’s disease, which suggests that steps to impede it may help treat or prevent it. Scientists state that medications might be developed to do just that. Mouse and cell-based experiments also lend credence to this line of hypothesis.
In reporting on scientists’ research on the subject, NIH reports, “They found over-expression of CD33 in support cells, called microglia, in postmortem brains from patients who had late-onset Alzheimer’s disease, the most common form of the illness. The more CD33 protein on the cell surface of microglia, the more beta-amyloid proteins and plaques—damaging debris—had accumulated in their brains.”
Rudolph Tanzi, Ph.D., a grantee of NIH’s National Institute of Mental Health, or NIMH, and the National Institute on Aging, NIA, stated, “Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.”
Tanzi worked on isolating the first familial Alzheimer’s disease gene, the amyloid b protein precursor, in 1987. He too was a key researcher in identifying two other FAD genes known as Presenilin 1 and 2 in 1995.
Tanzi is chairman of the Cure Alzheimer’s Fund Research Consortium and serves on over 50 editorial and scientific advisory boards. He is affiliated with Massachusetts GeneralHospital and was selected for “The Harvard 100: Most Influential Alumni”. Tanzi also was a cofounding scientist of Prana Biotechnology in 1997.
Prana works to develop therapeutic drugs for treating age-associated, brain and eye degeneration. Prana has reported significant findings recently in advancing the fight against both Alzheimer’s and Parkinson’s, including evidence for targeting specific metal imbalances in the brain to ameliorate Alzheimer’s pathology. Prana also has investigated intervention in metal dependent pathways in cases of Parkinson’s, preventing the death of substantia nigra cells and perhaps leading to improvements in motor function and coordination.